LH interacts with receptors on Leydig cells to stimulate a membrane-bound adenylate cyclase (Fig. 11.5). cAMP is subsequently released into the cytoplasm where it binds to a protein kinase.
Activation of the protein kinase, operating through unidentified intermediate steps, stimulates the conversion of cholesterol to pregnenolone. The control of LH operates primarily by negative feedback, and both testosterone and oestradiol can inhibit LH secretion. Testosterone can be converted to oestradiol in the brain, but the two hormones are believed to act independently on LH secretion. Testosterone slows the hypothalamic pulse generator in the hypothalamus and thus decreases the frequency of pulsatile LH release. It also exerts a negative feedback effect on LH secretion directly at the pituitary level.
